Greatly increased luminal nitric oxide in ulcerative colitis

Lundberg, Jon O.; Lundberg, Jan M.; Alving, Kjell; Hellström, Per M.

doi:10.1016/s0140-6736(94)90460-x

Cited by 232 publications

(159 citation statements)

References 6 publications

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“…In contrast, patients with active ulcerative colitis [58] or Crohn's disease [24,59] showed greatly increased luminal NO levels. The source of this NO is probably the mucosa, since increased NOS activity has been detected there by indirect methods in ulcerative colitis patients [60].…”

Section: Large Intestinementioning

confidence: 89%

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Nitric oxide in exhaled air

Lundberg¹,

Weitzberg²,

Lundberg³

et al. 1996

Eur Respir J

137

110

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Much interest is now being focused on measurements of nitric oxide (NO) in exhaled air. In healthy subjects exhaled NO seems to originate mainly in the nasal airways, whereas the contribution from the lower respiratory tract is low.In certain inflammatory airway disorders, the excretion of NO into the airways is altered resulting in changes in the levels of NO in exhaled air. New techniques have been developed to measure NO release at different levels of the airways: asthmatics show increased orally-exhaled NO levels, whereas patients with cystic fibrosis or Kartagener' 's syndrome exhibit a marked reduction in nasal release of NO. It has been suggested that measurements of exhaled NO may be clinically useful in noninvasive diagnosis and monitoring of inflammatory airway diseases.To further evaluate the potential clinical usefulness of measurement of exhaled NO, it is vital to explore how airway NO production is normally regulated and what factors influence airway NO excretion.

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Section: Large Intestinementioning

confidence: 89%

“…Low levels of NO have been found in gas aspirated from the colon of controls during colonoscopy [58]. In contrast, patients with active ulcerative colitis [58] or Crohn's disease [24,59] showed greatly increased luminal NO levels.…”

Section: Large Intestinementioning

confidence: 99%

Nitric oxide in exhaled air

Lundberg¹,

Weitzberg²,

Lundberg³

et al. 1996

Eur Respir J

137

110

View full text Add to dashboard Cite

show abstract

“…In local inflammatory diseases, NO from the gut lumen is markedly increased [30]. In porcine inflammatory models, NO release from the gut is unchanged [14] or even reduced [15].…”

Section: Discussionmentioning

confidence: 99%

Exhaled NO and plasma cGMP increase after endotoxin infusion in healthy volunteers

Soop¹,

Sollevi²,

Weitzberg³

et al. 2003

Eur Respir J

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Nitric oxide (NO) is believed to be involved in the pathophysiology of sepsis. This study evaluated the activity of the NO pathway in a human endotoxin model.At baseline and after endotoxin, on-line measurements of exhaled NO (eNO) were made using a chemiluminescence technique with a single-breath method. NO-free air was inhaled prior to exhalation against a resistance. NO in orally and nasally exhaled air and in rectal gas was investigated. Plasma nitrite, nitrate, and guanosine 39, 59-monophosphate (cGMP) and the events after diclophenac administration were also studied.Endotoxin infusion resulted in tachycardia and fever. An early increase in oral eNO concentration was observed and oral eNO decreased after diclophenac administration. NO exhaled nasally, NO in rectum gas and nitrite/nitrate levels remained unchanged over the study period. cGMP increased after 4 h.These findings suggest an early increase in nitric oxide production from the lungs, probably due to increased activity of the constitutive nitric oxide synthase upon endotoxin stimulation. In contrast, nitric oxide production in the upper airways, measured as nasally exhaled nitric oxide and nitric oxide in rectal gas, remained unchanged. Further studies will elucidate if exhaled nitric oxide is a valuable marker of sepsis-induced lung injury and if monitoring of treatment is possible. Eur Respir J 2003; 21: 594-599.

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“…mucus; bacteria; inflammatory bowel diseases; goblet cells SEVERAL FACTORS HAVE BEEN implicated in the pathogenesis of human inflammatory bowel diseases (IBD) including an immunological intolerance to enteric microflora (10 -12, 43), as well as defects in mucosal barrier function (47). Recently, attention has been focused on the overproduction of nitric oxide (NO) in IBD (7,31,46,58). Several studies have identified increased levels of NO in the rectal dialysates (46), in the inflamed mucosa of patients with ulcerative colitis (UC) (3), and in animal models of colitis (26,37,60).…”

mentioning

confidence: 99%

“…Recently, attention has been focused on the overproduction of nitric oxide (NO) in IBD (7,31,46,58). Several studies have identified increased levels of NO in the rectal dialysates (46), in the inflamed mucosa of patients with ulcerative colitis (UC) (3), and in animal models of colitis (26,37,60).…”

mentioning

confidence: 99%

Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity

Vallance¹,

Dijkstra²,

Qiu³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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The role of nitric oxide (NO) in inflammatory bowel diseases has traditionally focused on the inducible form of NO synthase (iNOS). However, the constitutive endothelial (eNOS) and neuronal (nNOS) isoforms may also impact on colitis, either by contributing to the inflammation or by regulating mucosal integrity in response to noxious stimuli. To date, studies examining the roles of the NOS isoforms in experimental colitis have been conflicting, and the mechanisms by which these enzymes exert their effects remain unclear. To investigate and clarify the roles of the NOS isoforms in gut inflammation, we induced trinitrobenzenesulfonic acid colitis in eNOS, nNOS, and iNOS knockout (KO) mice, assessing the course of colitis at early and late times. Both eNOS and iNOS KO mice developed a more severe colitis compared with wild-type mice. During colitis, iNOS expression dramatically increased on epithelial and lamina propria mononuclear cells, whereas eNOS expression remained localized to endothelial cells. Electron and fluorescence microscopy identified bacteria in the ulcerated colonic mucosa of eNOS KO mice, but not in wild-type, iNOS, or nNOS KO mice. Furthermore, eNOS KO mice had fewer colonic goblet cells, impaired mucin production, and exhibited increased susceptibility to an inflammatory stimulus that was subthreshold to other mice. This susceptibility was reversible, because the NO donor isosorbide dinitrate normalized goblet cell numbers and ameliorated subsequent colitis in eNOS KO mice. These results identify a protective role for both iNOS and eNOS during colitis, with eNOS deficiency resulting in impaired intestinal defense against lumenal bacteria and increased susceptibility to colitis. mucus; bacteria; inflammatory bowel diseases; goblet cells SEVERAL FACTORS HAVE BEEN implicated in the pathogenesis of human inflammatory bowel diseases (IBD) including an immunological intolerance to enteric microflora (10 -12, 43), as well as defects in mucosal barrier function (47). Recently, attention has been focused on the overproduction of nitric oxide (NO) in IBD (7,31,46,58). Several studies have identified increased levels of NO in the rectal dialysates (46), in the inflamed mucosa of patients with ulcerative colitis (UC) (3), and in animal models of colitis (26,37,60). The increased NO synthase (NOS) activity was identified predominantly as the inducible form of NOS (iNOS) (23). Whereas the two constitutive isoforms, neuronal (nNOS) and endothelial-derived (eNOS), modulate several aspects of intestinal physiology (6, 53), their contribution to the inflammatory response has received less attention.Despite considerable evidence that iNOS-derived NO contributes to tissue destruction in colitis and other inflammatory states (27), conflicting results have been obtained by using pharmacological inhibitors of NOS in animal models of IBD. Several studies have found that the nonspecific NOS inhibitor N G -nitro-L-arginine methyl ester reduced intestinal inflammation (17, 37, 45); other studies found little benefit (20) o...

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Greatly increased luminal nitric oxide in ulcerative colitis

Cited by 232 publications

References 6 publications

Nitric oxide in exhaled air

Nitric oxide in exhaled air

Exhaled NO and plasma cGMP increase after endotoxin infusion in healthy volunteers

Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity

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